The circadian system in patients with primary affective disorder is disorganized. A major symptom of this disease includes a disturbed activity-rest cycle. Treatments which affect the circadian system may correct a pathological state which underlies depression. Our goal is to understand how antidepressant chemicals alter the dynamics of the mammalian circadian system. Results from these studies will be valuable to understand the mechanism of chemical antidepressant treatments in humans. Previously we reported that in hamsters, clorgyline, a monoamine oxidase inhibitor with antidepressant properties, increases the period of the circadian clock and decreases the rest component of the daily activity-rest cycle. We also observed that this chemical alters the response of the circadian clock to light. These results indicate that clorgyline exhibits input properties to the circadian clock; the location of its input has been unclear. Processing of light information to the clock occurs at either the retina or the lateral geniculate nucleus projection to the clock. Results from the past year indicate clorgyline's effects are not mediated via the retinal projection to the clock. Our current hypothesis is that clorgyline alters the hamster circadian system via a lateral geniculate nucleus projection to the circadian clock. We are currently testing this hypothesis.